Dorsal sensory neurons convey to the spinal cord visceral and somatic sensory information which is crucial for sensation and for the regulation of motor functions. Neural pathways descending from the brain project not only to motor cells but also to sensory cell groups in the spinal cord, and regulate the processing of sensory messages there. Understanding the synaptic biochemistry of these fibers furthers the comprehension of normal and abnormal processing of somatosensory messages and encourages the construction of rational therapeutic approaches to abnormal sensory processing which accompanies some neural disorders. Although the synaptic transmitters of some dorsal sensory neurons are known, those used by most of these cells remain unidentified. Our previous studies suggest that dorsal sensory neurons use glutamate (L-GLU) or aspartate (L-ASP) as a transmitter. In microscope autoradiographic studies, we intend to determine which morphological types of dorsal sensory neuron use these compounds by observing which of them become labeled retrogradely after 3H-D-aspartate (D-ASP), a non-metabolizable marker of glutamatergic and aspartatergic neurons, is injected into the spinal gray. In biochemical studies, we intend to determine if dorsal sensory neurons use L-GLU, L-ASP, or both as transmitters by comparing the deficits in the synaptic release of these compounds from the spinal cord, in vitro, after cutting dorsal roots. Our preliminary studies also suggest that L-GLU or L-ASP may be a transmitter of one or more of tracts descending from the brain to the spinal cord. In biochemical studies, we intend to identify descending tracts that use these transmitters by observing if interruption of individual tracts in the spinal cord produces deficits in the uptake and release of the marker, D-ASP, and in the levels of endogenous L-GLU or L ASP in the dorsal horn of the spinal cord caudal to the lesion. In microscope autoradiographic studies, we intent to determine which descending tracts use L-GLU or L-ASP as transmitters by observing which of them become labeled retrogradely after D-ASP is injected into the spinal gray. To verify the identification of glutamatergic and aspartatergic destroyed in an attempt to mimic the deficits in biochemical activities observed after the appropriate spinal lesion.